通过Toll样受体5发出的信号可启动小鼠成骨细胞产生炎症介质。

Signaling via Toll-like receptor 5 can initiate inflammatory mediator production by murine osteoblasts.

作者信息

Madrazo Denise R, Tranguch Susanne L, Marriott Ian

机构信息

Department of Biology, University of North Carolina at Charlotte, Charlotte, North Carolina 28223, USA.

出版信息

Infect Immun. 2003 Sep;71(9):5418-21. doi: 10.1128/IAI.71.9.5418-5421.2003.

DOI:10.1128/IAI.71.9.5418-5421.2003

PMID:12933896

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC187346/

Abstract

Murine osteoblasts express Toll-like receptor 5 (TLR5), and this expression is upregulated following exposure to bacteria or to the TLR5 agonist, flagellin. Importantly, flagellin activates transcriptional regulators and elicits proinflammatory cytokine production, suggesting TLR5 functionality. TLR5 may represent an important mechanism underlying the recognition of bacterial pathogens by osteoblasts during bone infections.

摘要

小鼠成骨细胞表达Toll样受体5（TLR5），在暴露于细菌或TLR5激动剂鞭毛蛋白后，这种表达会上调。重要的是，鞭毛蛋白激活转录调节因子并引发促炎细胞因子的产生，表明TLR5具有功能。TLR5可能是骨感染期间成骨细胞识别细菌病原体的重要潜在机制。